Myocardin a enhances telomerase activities in adipose tissue mesenchymal cells and embryonic stem cells undergoing cardiovascular myogenic differentiation.
Madonna R., Willerson JT., Geng YJ.
Animal Study on Cardiovascular Disease, published in Stem Cells (2007) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Stem Cells (2007)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 17916802
- DOI
- 10.1634/stemcells.2007-0490
Abstract (original English)
Acting as a reverse transcriptase that maintains nuclear telomere length and replication potential, telomerase usually decreases in expression and activities when mammalian stem cells undergo terminal differentiation. This study identified, in adult adipose tissue, a subpopulation of mesenchymal stem cells (MSCs) that coexpresses telomerase and myocardin A, a key regulator of cardiovascular myogenic development. The telomerase/myocardin A-positive MSCs differentiated into cardiovascular myogenic cells while retaining expression and activation of the telomerase catalytic unit, telomerase reverse transcriptase (TERT), at a level comparable to that of ESCs. Both myocardin A and TERT could be coimmunoprecipitated from the developing MSCs and ESC-derived EBs with either anti-TERT or anti-myocardin A antibodies, suggesting the formation of TERT-myocardin A complexes in the MSCs and EBs. The proteins pulled down with anti-myocardin antibodies showed almost the same levels of telomerase activities as those precipitated with anti-TERT antibodies. Overexpression of myocardin A by cDNA transfection significantly increased telomerase activities and promoted telomere synthesis by MSCs. The data from this study indicate a potentially novel function of myocardin A in maintaining the myogenic stemness in developing MSCs and EBs by enhancing telomerase activation and promoting myogenic gene exp
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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